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    Home > Medical News > Medical Research Articles > One thing drops one thing!

    One thing drops one thing!

    • Last Update: 2021-07-25
    • Source: Internet
    • Author: User
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    TP53 is a key tumor suppressor gene
    , which is usually inactivated by missense mutations in the DNA binding domain.
    These missense mutations usually make p53 lose its tumor suppressor activity, and at the same time produce a mutant p53 that can promote tumor progression (mtp53).
    ) Protein

    The presence of mtp53 can increase chromosome instability, leading to the loss of tumor suppressor genes and the amplification of oncogenes


    Recently, researchers from the Luis A Martinez project of Stony Brook University in the United States
    published a study titled Mutant p53 suppresses innate immune signaling to promote tumorigenesis in
    Cancer Cell , and found that mtp53 can inhibit innate immune signaling, thereby Causes immunity to escape .
    Restoring TBK1 signal can bypass mtp53 and restore the function of immune cells, eradicating cancer cells .

    To determine whether mtp53 regulates innate immune signaling pathways, the researchers first down-regulated the expression of mtp53 in human breast cancer cells BT549 (p53R249S), MDA-MB-231 (p53R280K) and pancreatic cell lines MIA PaCa

    The results show that knocking down mtp53 can promote the phosphorylation of TBK1 and its substrates IRF3 and STING, which produce similar phenomena in both mouse and human cells

    Moreover, in two different types of normal human fibroblasts, IMR-90 and human foreskin fibroblasts, overexpression of mtp53 can reduce the phosphorylation of TBK1 and its substrates IRF3 and STING

    These results indicate that
    mtp53 blocks the activity of innate immune signaling pathways

    In the tumor microenvironment, the TBK1/STING/IRF3 pathway signals the presence of tumor cells to immune cells

    Researchers have found that
    mtp53 can block the nuclear translocation of IRF3, inhibit the innate immune response of cells in the cGAS/STING/TBK1/IRF3 pathway, and thereby inhibit IRF3-induced apoptosis
    Mtp53 can also interfere with the formation of the TBK1-STING-IRF3 complex, which can inhibit immune surveillance in a host with an intact immune system, thereby accelerating tumor growth

    Knockdown of mtp53 can promote the infiltration of CD3+, CD4+, CD8+ cells and NK cells


    Interestingly, the researchers found that
    activating TBK1 can inhibit mtp53-induced tumor growth and restore immune surveillance
    In other words, mtp53 induces inactivation of innate immune signals, changes the production of cytokines, and leads to immune escape; however,
    restoring TBK1 signals is sufficient to bypass mtp53, thereby restoring immune cell function and eradicating cancer cells

    In general, the study found a new mechanism.
    Mtp53 inhibits cell-autonomous and non-cell signaling by interfering with the function of the cytoplasmic DNA sensing mechanism cGAS-STING-TBK1-IRF3, thereby promoting cancer cell growth and evading immune surveillance.

    Restoring TBK1 signal can bypass mtp53, restore immune cell function, activate immune surveillance, and eradicate cancer cells

    This is of great significance.
    The status of p53 can guide treatment and provide new therapeutic targets


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